Botulism is a neuromuscular disorder of horses caused by neurotoxins of the bacteria Clostridium botulinum.
It results in flaccid paralysis by the action of the various botulinum neurotoxins.
The disease is also known as shaker foal syndrome, forage poisoning, and grass sickness.
Of the three types, botulism Type B occurs throughout the United States but is more predominant in the Mid-Atlantic states and Kentucky. Type A botulism occurs primarily in the west, while botulism type C occurs in Florida.
Botulism neurotoxins type B and C are the most commonly reported types in foals.
Botulism results from exposure to the toxin by three main routes, according to Dr Pamela Wilkins, of the University of Illinois College of Veterinary Medicine.
Ingestion of pre-formed toxin is the most common form affecting adult horses when they eat feed, such as hay or grain, that contains animal remains, Wilkins says.
“Swallowing the botulism organism with subsequent elaboration of toxin in the intestines is known as shaker foal syndrome, which is associated with one- to three-month-old foals, but can occur as early as one week of age,” she writes in Equine Disease Quarterly.
“Rarely, wound infection with Clostridium botulinum occurs and the subsequent release of the toxin in the body causes disease.”
Clinical signs after exposure to toxin occur from 12 hours to several days and may be dependent on dose and type of botulinum neurotoxin involved.
Sudden, unexplained death of one or more horses may be the initial signal of an outbreak, she says. Decreased eyelid, tongue, and tail tone may be observed early in disease. Horses that can walk may have a stilted, short-strided gait without poor coordination, she says.
Muscle trembling and weakness may be apparent, particularly in foals.
Pupillary dilation with sluggish pupillary light reflexes and difficulty swallowing is frequently observed.
Clinical signs may rapidly progress to animals being unable to stand. A fast heart rate may occur, particularly in foals. Death is generally attributed to respiratory failure secondary to respiratory muscle paralysis.
Diagnosis is made based on clinical signs. Definitive diagnosis requires detection of the toxin in serum, feces, gastrointestinal contents, or feed by one of several available tests.
Specific toxin activity can be confirmed by a mouse inoculation test and is supported by isolation of C. botulinum from serum, feces, gastrointestinal contents, or feed.
Treatment consists of blockade of any circulating toxin by intravenous administration of plasma containing specific antibotulism neurotoxin antibodies (generally against types B and/or C).
Supportive care, including fluid, nutritional, antimicrobial and respiratory supportive therapies, is critical.
Adults and foals with mild respiratory signs can frequently be treated with intranasal oxygen insufflation and positioning in sternal recumbency. Mechanical ventilation can be life-saving in foals.
Antimicrobial administration (avoiding procaine penicillin, aminoglycosides, and tetracyclines) is employed to prevent or reduce complications of the disease, such as aspiration pneumonia caused by dysphagia.
Nutritional management can be provided to foals by feeding milk or milk replacer via indwelling nasogastric or nasoesophageal tubes while in adult horses, periodic nasogastric intubation of slurry meals or commercially available liquid diets can be provided.
For type B botulism, the survival rate in appropriately treated foals less than six months of age is greater than 90 percent.
Affected adult horses that remain standing have a good prognosis, although a prolonged recovery, while recumbent adults are less likely to survive.
Vaccination with Clostridium botulinum type B toxoid is thought to be almost 100 percent protective against type B in adult horses and should be undertaken in endemic regions.
Vaccination of pregnant mares will be at least partially protective to their foals assuming adequate passive transfer of immunity.
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